Retracted: Upregulated microRNA‐485 suppresses apoptosis of renal tubular epithelial cells in mice with lupus nephritis via regulating the TGF‐β‐MAPK signaling pathway by inhibiting RhoA expression

Abstract

Lupus nephritis (LN) is a common and severe complication of systemic lupus erythematosus. Without intervention, LN may cause acute kidney injury and end-stage renal disease. This study aims to determine whether microRNA-485 (miR-485) affects renal tubular epithelial cells (RTECs) in LN mice via the TGF-β-MAPK signaling pathway by targeting RhoA. Renal tissue samples were initially extracted from 15 LN and 15 normal mice. RTECs were cultivated in vitro and grouped after transfection of different mimics, inhibitors, or siRNA- RhoA. The target gene of miR-485 was confirmed by dual-luciferase reporter assay. Flow cytometry and MTT assay were applied to detect cell viability and apoptosis. It was determined that RhoA was a target gene of miR-485. We found that urine protein, creatinine, RhoA, interleukin 6 (IL-6), transforming growth factor-β1 (TGF-β1), and p38 mitogen-activated protein kinases (p38MAPK) were highly expressed in renal tissues of LN mice, while poor levels of miR-485 were recorded. The overexpression of miR-485 or siRNA- RhoA or the combination of miR-485 and siRNA- RhoA was demonstrated to lead to a reduction of levels of RhoA, IL-6, TGF-β, and p38MAPK, as well as a promotion of RTECs proliferation and inhibition of RTECs apoptosis. Taken together, these findings indicated that overexpressed miR-485 downregulates RhoA which could promote cell viability and inhibit apoptosis of RTECs by regulating the RhoA-mediated TGF-β-MAPK signaling pathway in LN mice.

miRNA-485 Regulates Th17 Generation and Pathogenesis in Experimental Autoimmune Encephalomyelitis through Targeting STAT3

“…HMCs with overexpression of miR-485 had reduced levels of proin ammatory factors (TNF-a, IL-1b, IL-6) [32]. As indicated by Tian et al, miR-485 overexpression decreased RhoA, which stimulated the proliferation of renal tubular epithelial cells (RTEC) but suppressed their apoptosis by modulating the RhoA-dependent TGF-β-MAPK pathway among lupus nephritis mice [31]. According to Wang et al, overexpressed miR-485 hinders cell proliferation and stimulates the airway smooth muscle cells (ASMCs) apoptosis via Smurf2-dependent TGF-β/Smads pathway among chronic asthma mice [44].…”

“…Roles of miR-485 have been identi ed in diabetic nephropathy progression and lupus nephritis mice, overexpression of miRNA-485 inhibits the production of proin ammatory cytokines [31,32]. MiR-485 exhibits down-regulation within CD4 + T cells in MS cases when compared with normal subjects [33].…”

Fasudil prevents liver fibrosis via activating natural killer cells and suppressing hepatic stellate cells

“…In accordance with this, we found that liver injury and liver fibrosis induced by repeated injection of TAA were prevented by Fasudil treatment (Figures 1 and 2 ). In addition, several studies have proved that RhoA/ROCK pathway activation promotes TGF-β1 secretion in several models[ 30 ]. As a RhoA/ROCK inhibitor, Fasudil inhibited the induction of TGF-β1 secretion in TAA-induced liver fibrosis, consistent with previous studies.…”

Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p

“…RhoA promoted the vitality of rat renal tubular epithelial cells (RTEC) in lupus nephritis (LN) mice and inhibited RTEC cell apoptosis. e key regulatory role of the RhoA/p38MAPK pathway in cell apoptosis has been determined [25].…”